Reposted fromm Health Impact News Daily

by ClarenceIntroduction
I am not raising money or selling anything. I have ALS and want to share things that have helped me.Philosophy
I think it’s important you know my philosophy before reading on. A wise man (my father) would always say to me when something was broken; “Fix it with what’s available to you! What do you have to lose by trying?”
That’s how I see my ALS. I have a choice. I can sit and wait for others, such as medical/research groups, to find a way to fix my problem, which hasn’t happened. Or, I can try with what is available to me.
That’s what I have chosen to do: to TRY! Fortunately, I’ve experienced improvements. Maybe the improvements are only 10% to 20%, but that’s more than I had before. I believe I can still get more, but it won’t happen unless I keep trying! If you feel that way too, please read on.Basic Data
I am 62 with FALS (Familial Amyotrophic Lateral Sclerosis); inherited from my mother who died in 1987, about 8 years after its onset. I began showing signs in early 2007, and was officially diagnosed with FALS in September, 2008.
Because I believed there was nothing I could do to change the outcome, I just sat down to wait for the end. Then in late 2009 I read some things that caused me to think, “Dad was right, what do I have to lose by trying something outside the box!”
I’ve been taking magnesium chloride/water mixture since September 15th of 2009. I currently take 4 ounces per day (2 in the morning and 2 in the evening). I also started taking coconut oil on October 31, 2009. I started with 4 tbsp. per day the first month. I then went to 6 the second month, and upped it to 8 the third month. One coconut oil webpage said 4 tbsp. per day was for “NORMAL” people. I didn’t think with ALS I was normal. I now take 9 tbsp. per day (3 at each meal mixed into my food.) This is the only way I can take it. Straight causes me throat problems!
After reviewing another coconut oil webpage I started massaging coconut oil on my bad leg twice a day. The result from December 16, 2010 to January 31, 2011 was a 3/8” thigh circumference increase and improved strength. This was surprising so I am now massaging the entire leg, ankle and foot, focusing on any sore spots.
Following are specific details.A. Before Taking Coconut Oil and Magnesium Chloride: (Nov. 4, 2009)

Difficulty walking due to weakness in right leg; had to use canes to walk.

Right leg felt asleep and non-responsive when walking or trying to move it.

Right thigh muscles shrunken so bones could be easily felt through muscles on underside.

Had “drop-foot”. Could not tip right foot up or down, nor pivot it side to side as much as left.

When sitting could not raise right thigh off the chair.

Extreme difficulty putting right shoe on.

Right ankle very purple and bruised almost all the way around it.

When lying face down on stomach with legs outstretched; unable to raise my right foot.

Extreme difficulty rolling over in bed because right leg could not move on its own.

Right leg could not push downward at all.

Very thick saliva at night.

Excessive yawning.

Nearly constant muscle vibrations in entire right leg; some in left leg and upper right arm.

Increased strength and size in front muscles of right thigh but still weakness in buttocks, back thigh muscles, and muscles affecting knee.

Left leg strength and size increased.

Can stand on right leg a little longer because it has gained strength.

Can move right foot and toes up and down, and tap foot to music.

Can pivot right foot inward and outward some.

When sitting; can pull right foot backwards, although not yet as far as the left.

When sitting; able to raise right thigh upward to put on pants.

Less difficulty putting right foot into a shoe.

Bruised appearance of right ankle almost gone.

When lying face down on stomach with legs outstretched; can begin to raise my right foot.

Normal yawning.

Can roll over in bed with minimum difficulty.

Can push downward with right leg.

Muscle vibrations in legs and right arm only happen occasionally and only during the day.

Still have slight twitching in right thigh and buttocks. (Hopefully it’s muscles waking up).

Conclusion
Thus far my ALS progression is much slower than my mother’s. For both of us the first muscles to be affected were the ones that allow you to run (buttocks, thigh, and knee muscles, etc.). At this time some of these muscles are still not responsive. The reason could be because the nerve cells are slow to wake up from their 2+ years of sleep!
I have had positive improvements from adding coconut oil and magnesium chloride to my diet. It’s the only change I’ve made. I believe the coconut oil and magnesium chloride has slowed, and partially reversed the progression of my ALS. Therefore, I plan to keep going on the diet. I also plan to continue massaging my right leg with coconut oil, and tracking my changes, good or not so good, monthly to see what happens! What do I have to lose?
NOTE: Although some information out there says coconut oil increases cholesterol levels, my January 2011 blood test levels were very good.Update 2012
According to my doctors my annual EMG on March 6th 2012 showed no changes from last year. They said the progression had either stopped or was almost stopped, and that I should keep doing what I’ve been doing!
Since taking these things I’ve had enough positive changes that my doctors are confused, because they know there is supposedly nothing that helps people with ALS. Now they say I have ”a form of ALS called Benign Monomelic Amyotrophy.” So I asked them if there was anything to help people with that disease, and they said NO. Then I asked “Why have some of my muscles gotten larger and stronger?” THEY HAVE NO ANSWER! All they say now is “keep doing whatever you’re doing.” So I am!!! I no longer have a drop-foot, no muscle cramps, etc. However, some of the first muscles to go have not responded yet, but I’m not giving up on them.
Here is my latest update:

Before:

As of Sept. 15, 2009

1. Difficulty walking due to weakness in right leg; had to use canes to walk.
2. Right leg felt asleep and non-responsive when walking or trying to move it.
3. Right thigh muscles shrunken so bones could be easily felt through muscles on underside.
4. RH thigh @ 14 1/4” & LH @ 15 3/8”
5. Weight @ 148 lbs
6. ALS Functional Measurements @ 18%
7. Drop-foot
8. Cannot tip right foot up or down, nor pivot it side to side as much as left.
9. Cannot move toes much at all.
10. When sitting cannot raise right thigh upward to put on pants.
11. Extreme difficulty putting on right shoe.
12. Right ankle very purple and bruised almost all the way around it.
13. Unable to raise right foot when lying face down on stomach with legs outstretched.
14. Extreme difficulty rolling over in bed because right leg cannot move on its own.
15. Right leg cannot push downward at all.
16. Excess and thick saliva primarily at night.
17. Excessive yawning.
18. Cannot walk on toes of right foot.
19. Normally have to get up twice during the night to go to the bathroom.
20. Cannot stand on right leg at all because the knee will give way.
21. When sitting cannot pull right foot backwards at all.
22. Mild insomnia
23. Moderate stiffness in right leg and foot.
24. Cramps in different areas of both legs
25. Spasms in different areas of both legs
26. Weakness in right buttocks, thigh, calf, ankle, foot, and toes
27. Weakness starting in both hands.

Current

As of April 3, 2012

1. Still have difficulty walking due to weakness in right leg, and use canes or crutches to walk.
2. Normal feelings in right leg, somewhat more responsive when walking, etc.
3. Increased strength and size in both legs, and can no longer feel bones through muscles.
4. RH thigh @15 5/8” & LH @ 16 7/8”
5. Weight @ 152.9 lbs
6. ALS Functional Measurements @ 13%
7. Slight drop-foot due to weak ankle muscles.
8. Can tip right foot up and down, and side to side, but not as much as left.
9. Can move toes up and down
10. When sitting am able to raise right thigh upward to put on pants.
11. Less difficulty putting on right shoe.
12. Right ankle no longer has bruised appearance anywhere on it.
13. Can beryl raise right foot when lying face down with legs outstretched.
14. Can roll over in bed with a minimum of difficulty.
15. Right leg can push down with some force.
16. No problems anytime with saliva.
17. Normal yawning.
18. Still cannot walk on toes on right foot.
19. Almost never need to get up at night to go to the bathroom.
20. Can stand on right leg a little longer because it has gained some strength.
21. When sitting can pull right foot backwards, although not yet as far as the left.
22. No insomnia
23. Mild stiffness in right leg and foot.
24. No cramps in either leg
25. No spasms in either leg
26. Still have some weakness in right buttocks, thigh, calf, ankle, foot, and toes.
27. No more weakness in either hand.

Monday, February 25, 2013

Reposted from Diet Heart Publishing

Diet Heart Myths

Q: Do we have more heart disease today because we’re living longer?A: No. Adult life expectancy in 1910 was the same as today. Average life expectancy in 1910 was just 45 years, but when you factor out infant mortality and young women who died giving birth, you were just as likely to reach age 75 as you are today. Q: Are diabetes, obesity and heart disease mostly hereditary?A: Diabetes, obesity and coronary heart disease were far less common in 1910 (per capita), and our genes don't change in 100 years. As an example, the lifetime risk of diabetes in 1910 was 1 in 30; today it is 1 in 3. What has changed in the U.S. is the quality of our food, especially the type of fat and the type of carbohydrate we are eating.Q: Were "Cave man” and traditional diets low in fat? A: No. Throughout the world, primitive peoples sought out and consumed fat from fish and shellfish, water fowl, sea mammals, land birds, insects, reptiles, rodents, bears, dogs, pigs, cattle, sheep, goats, game, eggs, nuts and milk products. (westonaprice.org/Abrams, Food & Evolution 1987)Q: Do vegetarians live longer? A: No. The all-cause annual death rate of vegetarian men is slightly more than that of non-vegetarian men (.93% vs .89%); the annual death rate of vegetarian women is significantly more than that of non-vegetarian women (.86% vs .54%) (Am J Clin Nutr 1982 36:873)Q: Will a vegetarian diet protect you against atherosclerosis? A: No. The International Atherosclerosis Project found that vegetarians had just as much atherosclerosis as meat eaters. (Lab Invest 1968 18:498)Q: Does the European country with the highest average cholesterol have the lowest life expectancy? A: No – just the opposite! Switzerland has the highest average cholesterol levels (264 mg/dl) and the highest life expectancy. The Russians have the lowest cholesterol levels and the lowest life expectancy. (Dr. Malcolm Kendrick, MONICA study).Q: Is heart disease is caused by cholesterol and saturated fat from animal products? A: No, heart disease has multiple, inter-related causes. During the steady increase in reported coronary heart disease (1920-1967), consumption of animal fats declined but consumption of hydrogenated and industrially processed vegetable fats increased dramatically. (USDA statistics) Q: Does saturated fat clog arteries? A: No. So-called blockage is a complex “patch,” including - dominantly - fibrous tissue. The fatty acid component found in artery "blockage" is mostly unsaturated (74%) of which 41% is polyunsaturated. (Lancet 1994 344:1195)Q: Is it true that Vitamin B12 can be obtained from certain plant sources such as blue-green algae and soy products?A: Vitamin B12 is not absorbed from plant sources. Modern soy products increase the body's requirement for B12. Liver (organ meat) is our best source of all B-complex vitamins. (westonaprice.org).Q: Is it true that for good health and long life, serum cholesterol should be less than 180 mg/dl?A: Not according to the American Heart Association journal Circulation! The all-cause death rate is higher in individuals with cholesterol levels lower than 180 mg/dl. (Circulation, 1992 86:3:1026-1029).Q: Do children benefit from a low-fat diet? A: No, children need a high fat, high cholesterol diet! Mother’s milk is the highest cholesterol food on earth. Children on low-fat diets suffer from growth problems, failure to thrive & learning disabilities. (Food Chem News 10/3/94).Q: Will a low-fat diet help you "feel better and increase your joy of living?" A: No, as with growing children, low-fat diets are associated with increased rates of depression, psychological problems, fatigue, violence and suicide. (Lancet 3/21/92 v339).Q: Is cholesterol made in the liver?A: Yes - but every cell in the body can make cholesterol (except nerve tissue). Because dietary cholesterol is poorly absorbed – 50 percent at best - the body relies on endogenous production for its cholesterol needs, 1200 to 1800 milligrams per day. (Dr. Mary Enig, PhD, lipid biochemist).Q: Are lard (the rendered fat from a pig) and chicken skin saturated fats?A: Actually, lard and chicken fat are 60 and 70 percent unsaturated, respectively. Like all food fats, lard and chicken fat are a combination of different fatty acids - saturated and unsaturated. Lard and chicken fat are dominantly monounsaturated oleic acid, the dominant fat in olive oil. The experts who warn us about fat have yet to take their first course in lipid biochemistry.Q: Are saturated fats animal fats?A: No, saturated fats are found abundantly in tropical oils (coconut and palm) and are also present in varying amounts in most plants. Olive oil, for example, is 15-16 percent saturated fat. Even flaxseeds contain saturated fat. Fats are universal; saturated stearic acid in butter is the same molecule as stearic acid in chocolate. (Dr. Mary Enig, PhD, lipid biochemist).Q: Are polyunsaturated fats “plant fats”?A: Polyunsaturated fats are also found in marine life, fish and animals. Excess highly processed polyunsaturated fats – incorporated into are tissues – can promote injury and inflammation. Inflammation in the artery walls leads to plaque build up and blood clots.Q: Is vegetable shortening such as Crisco better than lard for a hearty health?A: Crisco shortening - hydrogenated vegetable fat made by Proctor & Gamble since 1912 – is harmful. For decades, Crisco has been a significant source of trans fatty acids in the American diet. Trans fats are not safe at any level. Lard from properly raised pigs is trans-free and is a great source of natural vitamin D.Q: Is Butter is more fattening than olive oil? A: No! Butter contains 15-17 percent short and medium chain fats that go right to the liver; not into our general circulation. Also, butter is 20 percent water. Olive oil is 100% fat and contains only long chain fats that circulate after digestion. Olive oil is potentially more “fattening” although fats do not make us fat unless they are part of a high carbohydrate diet.Q: Does butter contain a lot of cholesterol? A: No – cholesterol is found in food in tiny milligram (mg) amounts. A pound of butter contains 985 mg of cholesterol - less than 1 gram. A tablespoon of butter contains only 30 milligrams of cholesterol - and only 1/2 is absorbed. You would have to eat two pounds of butter daily in order to turn off the body’s own cholesterol synthesis.Q: Does high cholesterol foods raise blood cholesterol? A: Another myth! There’s no evidence that cholesterol in food raises cholesterol in blood – other than the positive result of promoting higher levels of beneficial HDL cholesterol. Towards the end of his life, Ancel Keys, the University of Minnesota professor who was first to blame cholesterol and fat on heart disease, said, "Cholesterol in food has no influence on cholesterol in blood and we've known that all along."Q: Does excess animal protein causes calcium to leach from the bones? A: No - the poorly conducted studies that make this false claim used dry protein powder – not fresh meat. Our bodies are made of protein and fat. We need optimum amounts of fresh protein and fat in order to rebuild and maintain our bodies. Q: Are excess dietary carbohydrates stored as carbohydrate? A: No, excess carbohydrates are turned into fat and stored as fat, especially in the abdomen, butt and thighs. Eat a lot of bread, cereal, pasta, juices and soft drinks and your body will turn it into fat. (Dr. Robert C. Atkins)Q: Is calcium is the most important mineral for the heart? A: No – and in excess - calcium becomes a bully – replacing magnesium is soft tissue throughout the body. “Hardening of the arteries” or calcification = too much calcium and not enough magnesium. It is unsafe to supplement with calcium unless you are taking equal amounts or more magnesium.Q: Are running and aerobic exercise good for the heart? A: Running and extreme exercise can be deadly! The number one cause of death among marathon runners is coronary heart disease. Runners tend to have enlarged hearts. Extreme exercise stresses the body and causes magnesium deficiencies. (Dr. William Campbell Douglas, MD)Q: Is health-food-store Canola oil a “good fat.”A: Canola (Canadian Oil) is made from genetically altered rapeseed. It is highly processed - subject to high temperature, high pressure. Canola contains small amounts of trans fat even though the label may say “trans fat free.” Canola in baked goods can promote mold growth that you cannot see.Q: Do cholesterol-lowering drugs reduce the incidence of heart failure?A: Just the opposite. Since approved in record-time in 1987, statin drugs are associated with a doubling of the incidence of heart failure.Q: Is heart-healthy L-Carnitine a reason to eat your veggies? A: No.Fruits, vegetables and grains are poor sources of Carnitine. Red meat is best, especially mutton, lamb and beef. The same is true for the important mineral zinc. Zinc is poorly absorbed from plants and easily absorbed from red meat. (Robert Crayhon)Q: To avoid heart disease, should we use margarine instead of butter?A: No, never eat margarine despite what manufacturers claim. Margarine eaters have twice the rate of heart disease as butter eaters. (Nutrition Week 3/22/91 21:12)Q: Does highly saturated coconut oil causes heart disease? A: No. Populations that consume coconut oil have low rates of heart disease. Coconut oil may also be one of the most useful oils to prevent heart disease because of its antiviral and antimicrobial characteristics. (JAMA 1967 202:1119-1123; Am J Clin Nutr 1981 34:1552)Q: Is it true that in 1977, a vegetarian researched and wrote the first U.S. Dietary Guidelines?A: Yes, a true statement! Mr. Nick Mottern, a vegetarian and former labor reporter for a Providence, RI newspaper, was hired by Senator George McGovern’s committee staff to write our first ever low fat Dietary Guidelines. (Gary Taubes, Good Calories, Bad Calories) Q: Heart-Healthy L-Carnitine is a reason to eat your veggies.

As its name suggests, macular degeneration is a degenerative condition of the macula, the area of the retina responsible for central vision. In some people, it is caused by excessive blood vessel growth and fluid leakage in the retina. This “wet” form, which is often treated with lasers or drugs to retard the growth of the abnormal vessels, is responsible for most macular degeneration–related blindness.
But the majority of people afflicted with macular degeneration have the “dry” type, which is marked by buildup of metabolic waste products in the macula. These lesions interfere with blood flow to the macula and impair function of light-sensitive cells. Dry macular degeneration progresses more slowly and results in less severe vision loss, although over time it can also cause significant impairment. Conventional medicine considers dry macular degeneration to be “untreatable,” but this just isn’t true.Here is the protocol I recommend for preventing and treating macular degeneration.

Eat plenty of leafy greens. Population studies reveal that people who eat an abundance of leafy greens have a reduced risk of macular degeneration. That’s because these vegetables are excellent sources of lutein and zeaxanthin—carotenoids that protect the retina by absorbing harmful wavelengths of light and scavenging free radicals. In one study, individuals who ate the most spinach, kale, collards, and other leafy greens had a 43 percent lower risk of developing macular degeneration compared with those who ate the least.

Have fish a few times a week. Omega-3 fatty acids in oily fish have also been shown to protect the retina. Australian researchers followed 2,335 people age 49 or older for five years and found that eating fish once a week lowered risk of early macular degeneration by 40 percent; three weekly servings lowered risk of advanced macular degeneration by 75 percent.

Supplement with antioxidants and a broad range of phytonutrients. The 10-year Age-Related Eye Disease Study proved that high doses of antioxidants (vitamins C and E, beta-carotene, and zinc) significantly reduced the risk of advanced macular degeneration and vision loss in patients with early-stage disease. And additional research has highlighted the benefits of a broad range of phytonutrients, including lutein and zeaxanthin. Another study found that postmenopausal women with high vitamin D levels are at significantly reduced risk of macular degeneration.

Suggested daily doses of eye-nourishing nutrients are 1,000 mg of vitamin C, 400 IU of vitamin E, 15,000 IU of beta-carotene, 50–80 mg of zinc, 15 mg of lutein, and 2 mg of zeaxanthin. You may need to combine a potent multivitamin with a vision-targeted formula to achieve these levels.

Consider a course of hyperbaric oxygen therapy (HBOT). HBOT involves breathing 100 percent oxygen in a pressurized environment. It works on two fronts to regenerate damaged tissues: It saturates the cells with oxygen, and it mobilizes stem cells, which can be transformed into a broad range of cell types. HBOT’s effects on macular degeneration can be dramatic. In one small study, the visual acuity of three patients treated with HBOT doubled, and a fourth patient’s nearly quadrupled.

Some age-related vision changes are to be expected. Virtually all of us will require reading glasses at some point in our lives. Macular degeneration, however, is not inevitable. It’s never too early to be proactive about your vision, especially if you are female, Caucasian, have light-colored eyes, smoke, are obese, or have a family history of macular degeneration, all of which place you at increased risk.
Take a hard look at your diet and make appropriate changes, start on a nutritional supplement program geared toward eye health, and you’ll be well on your way toward a lifetime of better vision.Now it’s your turn: Do you take supplements targeted at vision health?

Reposted from LabSpaces

Neuroscientist Patrik Verstreken, associated with VIB and KU Leuven, succeeded in undoing the effect of one of the genetic defects that leads to Parkinson's using vitamin K2. His discovery gives hope to Parkinson's patients. This research was done in collaboration with colleagues from Northern Illinois University (US) and will be published on the website of the authorative journalScience.
"It appears from our research that administering vitamin K2 could possibly help patients with Parkinson's. However, more work needs to be done to understand this better," says Patrik Verstreken.
Malfunctioning power plants are at the basis of Parkinson's.
If we looked at cells as small factories, then mitochondria would be the power plants responsible for supplying the energy for their operation. They generate this energy by transporting electrons. In Parkinson's patients, the activity of mitochondria and the transport of electrons have been disrupted, resulting in the mitochondria no longer producing sufficient energy for the cell. This has major consequences as the cells in certain parts of the brain will start dying off, disrupting communication between neurons. The results are the typical symptoms of Parkinson's: lack of movement (akinesia), tremors and muscle stiffness.
The exact cause of this neurodegenerative disease is not known. In recent years, however, scientists have been able to describe several genetic defects (mutations) found in Parkinson's patients, including the so-called PINK1 and Parkin mutations, which both lead to reduced mitochondrial activity. By studying these mutations, scientists hope to unravel the mechanisms underlying the disease process.
Paralyzed fruit flies
Fruit flies (Drosophila) are frequently used in lab experiments because of their short life spans and breeding cycles, among other things. Within two weeks of her emergence, every female is able to produce hundreds of offspring. By genetically modifying fruitflies, scientists can study the function of certain genes and proteins. Patrik Verstreken and his team used fruitflies with a genetic defect in PINK1 or Parkin that is similar to the one associated with Parkinson's. They found that the flies with a PINK1 or Parkin mutation lost their ability to fly.
Upon closer examination, they discovered that the mitochondria in these flies were defective, just as in Parkinson's patients. Because of this they generated less intracellular energy – energy the insects needed to fly. When the flies were given vitamin K2, the energy production in their mitochondria was restored and the insects' ability to fly improved. The researchers were also able to determine that the energy production was restored because the vitamin K2 had improved electron transport in the mitochondria. This in turn led to improved energy production.
Conclusion
Vitamin K2 plays a role in the energy production of defective mitochondria. Because defective mitochondria are also found in Parkinson's patients with a PINK1 or Parkin mutation, vitamin K2 potentially offers hope for a new treatment for Parkinson's.
###
VIB (the Flanders Institute for Biotechnology): http://www.vib.be

Reposted from Life Extension

Mounting evidence documents the ability of carnosine to prevent many of the detrimental effects of aging.1
In our youth, carnosine shields us from the onslaught of oxidation, glycation, DNA damage, and other reactions that injure tissues and cripple organs.1
The problem is that as we grow older, carnosine levels in the body decline,2-4 leaving us vulnerable to loss of cognitive function, decreased mobility, loss of metabolic control, failing cardiovascular performance, and an increased susceptibility to cancer.
In laboratory animals of different species, carnosine supplementation extends life spans. This is all adding up to a new era in the way conventional medicine thinks about aging.

Scientists Explore Carnosine’s Longevity Benefits

Carnosine is found throughout the body wherever there are high energy demands such as in the brain, the heart, and our muscles.5 Its function is to protect these vital areas from the metabolic demands of energy production and management.6,7
Young organisms have high levels of carnosine in those energy-demanding tissues. As part of the aging process, carnosine levels decline over time.2-4 That’s because our bodies both make less carnosine as we age, and also because the carnosine we have is increasingly vulnerable to destruction. In human conditions such as diabetes and metabolic syndrome, which produce unnaturally accelerated aging, carnosine production is decreased, and its destruction is increased.8,9
These findings suggest that a “carnosine deficiency” might be partly responsible for the visible aging and loss of function in a multitude of areas throughout the body that occurs as we get older.
If we could restore our bodies’ carnosine stores to their youthful levels, we might be able to arrest part of the aging process.
Here are a few of the most dramatic observations in recent years that demonstrate how carnosine supplementation extends life spans:

Carnosine slows the aging of human cells in culture dishes.10,11 Scientists added carnosine to cultures of young cells. While the control cells developed the typical “old” appearance, those grown in high carnosine concentrations retained their youthful appearance.5 When these youthful-appearing cells were transferred to culture dishes lacking extra carnosine, they quickly developed the “old” appearance of control cells of the same age. Yet, when scientists took old cells, approaching the limits of their life span, and transferred them into culture dishes containing high carnosine concentrations, they found that the cells rapidly became rejuvenated to resemble young cells.10

Carnosine extends the life span of rotifers, a microscopic aquatic organism now being used as a model of aging in many laboratories.12 In this experiment, scientists tested many different antioxidant compounds, identifying carnosine as one of just four that had significant effects on the organisms’ longevity.

Carnosine extends the life span of fruit flies, another organism commonly used to study aging, up to 20% in males.13,14 Normally, male fruit flies die much sooner than do females, but when fed a steady diet including a carnosine supplement, the males attained the same age as the females.

Carnosine extends the life span of laboratory mice, complex, warm-blooded mammals with many of the aging features common to humans.15,16

Scientists used a strain of mice in which aging is markedly accelerated and supplemented their food with carnosine. Not only did the animals live significantly longer, they retained the physical and behavioral features of youthful animals.15 Next, the scientists tested the supplement in normal mice, finding much the same effects. Carnosine clearly improved the animals’ external appearances and maintained the animals in better condition than control animals receiving no carnosine.16

What You NEed To Know: Carnosine Provides Broad-Spectrum Defense Against Aging

Carnosine supplementation can restore youthful carnosine levels in blood and tissues, and it extends the life spans of experimental animals of many species.

Carnosine supplementation may protect against neurodegenerative diseases and stroke; it also enhances exercise performance and comfort, ameliorates diabetes and its complications, and protects heart muscle and blood vessels from atherosclerosis.

Carnosine Protects Against Cardiovascular Disease

Carnosine’s multi-targeted effects are most prominent in the heart and blood vessels. Carnosine has been shown to decrease mortality from strokes as well as mitigate the damaging effects of stroke on the brain itself.17-19 Studies in experimental animals show that carnosine, administered before or after a stroke is induced, protects brain cells from the so-called ischemia-reperfusion injury that occurs when tissue is first deprived of oxygen and is then subjected to high oxygen levels when blood flow is restored.17,18 That results in marked reduction in signs of oxidant damage to brain cells, and to a real and significant reduction in the size of the stroke area in the brain.18
Carnosine also protects heart muscle from ischemia (lack of blood flow), which can ultimately produce a heart attack. This protection derives from carnosine’s antioxidant actions, combined with its ability to trap oxidation-inducing transition metals, its acid-buffering capacity, and its influence on inflammatory cell activity.19 In fact, carnosine has been added to solutions used to protect heart muscle during open-heart surgery, when the heart is intentionally stopped, and there is high risk for ischemic damage.20
Carnosine’s actions on blood vessels may even prevent ischemia from occurring in the first place. Carnosine protects artery-lining endothelial cells from oxidation and glycation, both of which are early events in development of atherosclerosis.21,22 Studies show that carnosine prevents formation of dangerous “foam cells,” fat-laden scavenger cells that trigger the inflammatory response that produces deadly arterial plaque.23
Excessive muscle tone in arteries raises blood pressure and reduces blood flow to heart muscle and brain cells; carnosine reduces arterial tone by multiple mechanisms.24 It modulates calcium ion signaling in the smooth muscle cells that control vascular tone and enhances production of beneficial endothelial nitric oxide synthetase (eNOS) that induces arteries to relax.25
Given carnosine’s beneficial impact on skeletal muscle and exercise performance, it is hardly surprising to learn that carnosine also enhances heart muscle contractility. This is again a multifactorial effect, produced in part by carnosine’s ability to control calcium flow, and partly by its antioxidant, acid buffering, and anti-glycation activities.19,26,27

Carnosine Fights Diabetes and Its Consequences

The global obesity epidemic brings with it the growing threat of type 2 diabetes and all of its devastating consequences that include cardiovascular disease, kidney failure, nerve damage, and eye disorders.
Studies show that diabetics’ cells have lower-than-normal carnosine levels, similar to levels in older adults.10 That may be one reason that diabetes produces accelerated aging.28
Yet carnosine supplementation can restore youthful carnosine levels in vital tissues, and offers protection against many of the components of diabetes.
Carnosine lowers elevated blood sugar levels, reduces long-term formation of dangerous advanced glycation end-products, limits oxidant stress and elevated inflammation, and prevents protein cross-linking, not only in diabetics, but also in otherwise healthy aging adults.29-33
Additionally, carnosine works ‘behind the scenes’ to offer important protection for diabetics’ physiological destruction from high blood sugar:

Carnosine protects kidney cells from the effects of high glucose levels, helping to reduce the risk of diabetic kidney disease, or nephropathy.34-36

Carnosine reduces oxidation and glycation of low-density lipoprotein (LDL) which bodes well for reduction of diabetes-induced atherosclerosis.37,23

Carnosine reduces protein cross-linking in the lens of the eye and helps to reduce the risk of cataract, a common diabetic complication.38,39

Carnosine supplementation also prevents the microscopic blood vessel damage that produces diabetic retinopathy, a major cause of blindness in diabetics.40

Carnosine Protects Brain Cells, Preserves Cognition

So far, drug treatment has shown only minimal effectiveness at slowing the progression of cognitive decline. Carnosine’s many therapeutic targets make it exceptionally promising for all of these conditions.42Alzheimer’s disease is the most widely feared and the most common of the neurodegenerative disorders. Scientists have found that Alzheimer’s patients have even lower levels of carnosine in their brains and spinal fluid than those of other older adults.43 It is not yet clear whether this is a cause or an effect of Alzheimer’s, but many intriguing observations suggest a role for carnosine in prevention of the disease.
Alzheimer’s disease is the result of multiple causes, virtually all of which have some connection to carnosine and its function in the brain. Noted expert Alan R. Hipkiss of London’s Queen Mary’s School of Medicine and Dentistry recently summarized the relationship between Alzheimer’s and falling levels of carnosine in the body.
Hipkiss observed that those parts of the brain that are first affected in early Alzheimer’s disease are also those in which carnosine is normally found in highest concentrations.44 That suggests that, as carnosine levels fall with age, those brain areas become the most vulnerable to the Alzheimer’s-related damage. In addition, he notes that the abnormal protein, amyloid beta, which is seen exclusively in Alzheimer’s diseased brains is typically full of zinc ions. Carnosine is capable of binding up zinc and keeping it from damaging tissues in excess.44,45 Again, the implication is that falling levels of carnosine allow brain tissue to fall victim to an unnatural accumulation of a toxic substance.
Finally, Hipkiss notes that the so-called “neurofibrillary tangles” found in the brains of Alzheimer’s disease patients contain proteins that are extensively cross-linked.44 Carnosine is an effective inhibitor of protein cross-linking everywhere in the body.46Mitochondrial dysfunction is yet another contributor to Alzheimer’s disease; the oxidant stress it produces may be involved in formation of the Alzheimer’s protein amyloid beta.47 Experimental studies show that supplementing Alzheimer’s disease mice with carnosine potently reduces amyloid beta accumulation and completely rescues their brains from mitochondrial dysfunction.31
These biochemical relationships are now showing real effects in experimental models of neurodegenerative diseases of aging. Researchers fed aged rats a supplement rich in carnosine, which also contained vitamin D3 as well as blueberry and green tea polyphenols, or a control substance.48 The animals were then trained in finding their way to a platform submerged in water. By the end of the training period, the treated group of impaired older animals performed better than the controls in the same age category. Supplemented animals also were found to have increased production of new brain cells and fewer markers of brain cell inflammation and deterioration than controls. Similar anti-oxidative and anti-inflammatory effects were seen in the brains of mice with an experimental form of Parkinson’s disease.49Strokes cause brain cells to die from oxidant damage. Recent studies show that carnosine’s antioxidant effects provide some protection against both ischemic stroke (in which too little blood reaches brain tissue), and hemorrhagic strokes (in which bleeding exposes brain tissue to damage from free blood).
In one study, rats were supplemented with a carnosine-blueberry-green tea-vitamin D3 mixture for two weeks prior to experimentally-induced ischemic stroke, at which time a major brain artery was surgically blocked.50 Pre- and post-surgery behavioral testing demonstrated that, compared with control animals, supplemented rats had a 12% reduction in motor asymmetry, and a 24% reduction in neurologic dysfunction following the stroke. Supplemented rats also had up to a 3-fold increase in new brain cell proliferation after the stroke, compared with controls.
Other studies of ischemic stroke demonstrate a strong reduction in oxidative stress and brain cell death by apoptosis in animals supplemented with carnosine.51 Importantly, carnosine also provides protection following ischemia from so-called glutamate excitotoxicity, the same sort of neuronal “overdrive” that is thought to further contribute to Alzheimer’s disease.52
In experimental models of hemorrhagic stroke, carnosine treatment led to restoration of normal neurotransmitter receptors damaged by the presence of blood in brain tissue.53 Carnosine also prevented some of the dangerous swelling that often follows a hemorrhagic stroke.53

Carnosine Targets Six Multiple Molecular Aging Mechanisms

Initially, researchers considered carnosine as just an antioxidant molecule. But, while it has good antioxidant effects, carnosine is by no means the most powerful antioxidant in the body. What caught the researchers’ attention was that supplementation with other, more potent, antioxidants did not produce the dramatic increase in longevity seen with carnosine.62,65
Clearly, something else is going on.
Few scientists, however, were prepared for the revelation that carnosine actually targets six major processes involved in the aging process. Let’s look briefly at each one, to see how carnosine exerts its overall effects.

Oxidation at the cellular and tissue levels is one of the major contributors to the aging of organisms. Carnosine scavenges oxygen and nitrogen free radicals, and reduces their destructive impact on fat and DNA molecules.1,62,66,67 These effects are a powerful means of stopping atherosclerosis and cancer formation, respectively.

Glycation, the formation of molecular compounds of glucose with vital biomolecules such as enzymes and other proteins, is another major cause of aging. Glycated proteins induce potent oxidant stress and trigger inflammatory responses that hasten the aging process. Glycated proteins also form “cross-links” that bind them together, reducing their youthful flexibility and function. Carnosine takes a “sacrificial hit” and allows itself to be glycated, sparing other vital structures and preventing dangerous protein cross-linking.5,67,68

Accumulation of excess metals44,69 Carnosine chelates, or binds to, ions of copper, zinc, and iron, which in excess are known to induce production of amyloid beta and other proteins found in Alzheimer’s and Parkinson’s diseases.66,70-72

Cross-linked proteinsare theresult of accumulated oxidant damage and glycationin youth. They are eliminated by intracellular structures called proteasomes.65 With increasing age, however, proteasomal degradation drops off, allowing the dysfunctional proteins to accumulate and interfere with cellular function. Carnosine can react with these abnormal proteins, hastening their elimination.65,70

Telomeresare the repeating DNA sequences at the ends of chromosomes that function as a kind of “molecular clock,” becoming shortened with each cycle of cell replication. When telomeres become too short, cells die. Carnosine reduces damage to telomeres and slows their rate of shortening in experimental systems.64

Mitochondrial dysfunction accelerates aging by depriving cells of the energy they need, and by adding to their oxidative burden as mitochondria lose their efficiency.73 Carnosine alleviates all of these alterations, especially in vulnerable brain cells where mitochondrial dysfunction contributes to Alzheimer’s and other neurodegenerative diseases.47,73,74

Carnosine Enhances Exercise Performance

While excess body fat increases the risk of diabetes, regular exercise reduces the risk of both obesity and diabetes. Carnosine supports exercise performance by buffering the rising levels of acid that accumulate in working muscle.55,56 Accumulating acid in muscles produces the fatigue and pain that ultimately limits our workouts.54,57,58
Increasing muscle carnosine levels is now a well-established means of improving exercise performance and reducing fatigue, both in trained and untrained individuals.6,59,60 In older adults, in whom frailty and the risk of falls increases with muscle weakness, it can be a critical factor in promoting safety and independent living.61
In one study of people 55-92 years old, raising muscle carnosine content increased their fatigue threshold by 29% from pre- to post-supplementation, with no change seen in the placebo group.62 A similar study among 60-80 year-olds demonstrated a significant increase in the time subjects could exercise before becoming exhausted.63

Summary

The past decade has led to a broad array of findings regarding carnosine’s multiple protective effects, arising from its ability to fight multiple processes that cause aging.
Carnosine defends against oxidant damage, glycation of vital proteins, acid accumulation in muscle and heart, dangerous transition metal ions, age-induced protein cross-linking, mitochondrial dysfunction, and age-accelerating telomere shortening.64
These multitargeted actions collaborate to prevent age-related diseases such as cognitive decline and dementia, to promote exercise comfort and performance, to slow progression of metabolic conditions such as diabetes, and to defend against atherosclerosis and heart disease. It’s no wonder carnosine is referred to as the “antiaging dipeptide.”26
If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.

As the kitchen filled with the smell of caramelised meat, my mouth watered in anticipation of the coming feast: a thick cut of tender steak, fried in butter and olive oil. This was not a regular treat. In fact, for the previous 26 years I’d been a vegan, eschewing not just meat but all animal products. My diet was an extreme version of the NHS Eat Well regime, which recommends lots of starchy foods and smaller quantities of saturated fats, cholesterol, sugar and red meat.

In 2010, John Nicholson decided to give up my supposedly healthy lifestyle and embrace good old-fashioned meat

According to government advice, I was doing everything right — and yet my health had never been worse. My weight had crept up over the years, until in 2008 I was 14½ stone — which is a lot of blubber for someone who is 5ft 10in — and was classified as clinically obese. I waddled around, sweating and short of breath, battling extremely high cholesterol and suffering from chronic indigestion. I was always tired and needed to take naps every afternoon. I had constant headaches and swallowed paracetamol and sucked Rennies like they were sweets.Worst of all, I had irritable bowel syndrome (IBS), which left me feeling as if I had lead weights in my gut. My belly was bloated and distended after every meal. I was, to use a technical term, knackered.But that was about to change. In 2010, I decided to give up my supposedly healthy lifestyle and embrace good old-fashioned meat.

From that day on, I ate red meat four or five days a week. I gobbled the fat on chops, chicken skin and pork crackling. I feasted on everything we’re told to avoid. The effects were instant.Twenty-four hours after eating meat again, all my IBS symptoms had gone. As the weeks and months passed, every aspect of my health improved dramatically. I became leaner, shedding body fat and becoming stronger and fitter. My headaches went away, never to return. Even my libido increased.It felt like being young again, like coming back to life. But though I felt energised, I was also furious.

Diet swap: John was fat and ill as a vegan, left, but is now the picture of health as a meat eater, right

Furious with myself for sticking to the ‘healthy’ eating advice, which was actually far from a sensible diet. But also furious with the so-called experts who have been peddling this low-fat, high-carbohydrate claptrap for so long that no one thinks to question it. My maternal grandmother would certainly have challenged it. Like my grandfather, she was born into a poor family in East Yorkshire at the turn of the century and their eating regime was simple: meat and at least two vegetables at every meal, lots of butter and full-cream milk (they would have scorned yogurt as little more than ‘off’ milk), bread, potatoes, cake and puddings.

Nothing would have swayed them from that lifestyle. Had a low-fat diet been suggested by a doctor, Gran would have told him to his face that it was all rubbish and that you needed fat to ‘keep the cold out’. If she could have seen people buying skimmed milk today, she would have thought they had lost their minds. Getting rid of the best bit of milk? Lunacy.Late in her life, I recall her scorning the advice on limiting the consumption of eggs because of concerns about cholesterol. On one occasion, she watched in astonishment as a celebrity TV chef made an egg-white omelette. ‘He’s a bloody fool, that man,’ she said.She was right to be sceptical, it turns out. For years the authorities told us cholesterol-rich foods would kill us — but we’ve since learned that is utter drivel. While Ancel Keys, the scientist whose research in the Fifties first raised concerns about cholesterol levels, suggested that heart disease was linked to large amounts of cholesterol in the blood, he never claimed those levels were linked to the amount of cholesterol we eat.‘There’s no connection whatsoever between cholesterol in food and cholesterol in blood,’ he said in a magazine article in 1997. ‘And we’ve known that all along.’Since then, the NHS’s paranoia about cholesterol in food has been replaced by concerns about saturated fat — found in everything from butter, cheese and cream to pies, cakes and biscuits.They suggest saturated fat increases the risk of heart disease. But this is open to debate. France has the lowest rate of death from coronary heart disease in Europe, yet the country has the highest consumption of saturated fats.Gran survived into her 80s and Grandad into his 70s, despite labouring down the pit his whole working life. Did they achieve this by gobbling low-fat spreads, soya oil or skimmed milk? No, they lived on old-fashioned foods such as butter, lard and beef fat. Indeed, a growing body of opinion suggests that the factory-made products that have replaced these staples — vegetable oils, polyunsaturated margarine and spreads — are the real cause of the degenerative diseases that are so common today.Findings by the Weston A. Price Foundation, a non-profit-making research organisation in America, show most cases of heart attack in the 20th century were of a hitherto little-known form known as myocardial infarction (MI) — a huge blood clot leading to the obstruction of a coronary artery.

Healthy: The NHS's paranoia about cholesterol in food has been replaced by concerns about saturated fat - found in everything from butter, cheese and cream to pies, cakes and biscuits

MI was almost non-existent in the U.S. in 1910 and was causing no more than 3,000 deaths a year by 1930. However, by 1960, there were at least 500,000 MI deaths a year across the country.It surely can’t be a coincidence that this happened as the U.S. embraced a new diet based on increasingly large portions of highly processed foods and vegetable oils?Similar changes in the national diet took place in Britain during the early years of my life and I can’t help wondering whether my father might still be alive today if it had not been for this shift.I grew up in the North-East during the Sixties and had no idea about ‘healthy eating’. Those few people who did fret about their diet were thought of as fussy.No one thought food was a problem, unless the chip shop ran out of battered sausage on a Friday. We ate suet puddings every week, our bacon and eggs were fried in lard, milk was full-fat — I’m not sure skimmed milk even existed in the Sixties — and we ate eggs every day.Then, in the Seventies, things changed. We got wealthier and food became cheaper. Mam began buying more cakes and confectionery instead of home-baking. We ate more shop-bought food in general.She also stopped using lard in the chip pan, opting for Spry Crisp ’n Dry instead. Gran wasn’t pleased. She thought vegetable oil was a new-fangled fad — it was, and that was precisely why Mam liked it. She saw it as moving on, modern and fashionable.

'I grew up in the North-East during the Sixties and had no idea about ‘healthy eating’

Dad never did any exercise and drove everywhere in his newly acquired company car. More processed food, margarine, sugar and vegetable oil, combined with days spent behind a desk and a wheel, saw him gain a sizeable belly and the apple shape so common today. In 1987, he died of a massive heart attack, aged just 65.His diet in his later years was not one that would have appealed to Gran. She was vehemently against margarine.‘I’m not eating anything made in a factory,’ she’d say. ‘You don’t know what they put in it.’It was a fear shared by many of her era. Had I heeded such warnings, I would have avoided my battle with processed food, in the form of soya, the bean whose industrially produced extracts are marketed as a low-fat and exceptionally healthy source of protein.Today, soya is everywhere. About two-thirds of all processed food in the U.S. contains some form of it.That percentage will not be much different here — you’d be amazed at how often you eat ‘hidden’ soya. When my partner, Dawn, and I decided to become vegan during the Eighties, it was still rare in Britain. This lifestyle shift came about shortly after we’d left Newcastle Polytechnic and moved to live self-sufficiently in a rented cottage in northern Scotland. When one of our chickens became ill, we found it terribly difficult to put it out of its misery and began to doubt whether killing — or eating — animals was for us. We didn’t see why someone else should have to do our dirty work for us, so in January 1984 we ate our last bacon sandwiches and embarked on our dramatic lifestyle change.At about this time, governments in the U.S. and Europe were recommending that people cut down on eating animal fats, cholesterol and red meat in favour of more starchy foods, fruit and vegetables and wholegrains.This new healthy eating advice had much in common with the vegetarian diet. We felt we were following a golden path, especially when we discovered the apparent wonders of soya.

In the Sixties people didn't fret about their diet and regularly tucked into food like fish and chips, suet puddings and bacon and eggs fried in lard